Inv(11)(q21q23); KMT2A-MAML2, a Recurrent Genetic Abnormality in T-Cell Therapy-related Acute Lymphoblastic Leukemia
| Autor: | Joanna Weinstein, Rachel A. Mariani, Kai Lee Yap, Shunyou Gong, Edward Caparelli, Lawrence J. Jennings, Katrin M. Leuer, Mercedes Silva |
|---|---|
| Rok vydání: | 2019 |
| Předmět: |
Male
Oncogene Proteins Fusion T cell Lymphoblastic Leukemia medicine.medical_treatment Disease Fusion gene 03 medical and health sciences 0302 clinical medicine hemic and lymphatic diseases Precursor B-Cell Lymphoblastic Leukemia-Lymphoma medicine Humans Chromosomal inversion Chemotherapy biology business.industry Chromosomes Human Pair 11 Neoplasms Second Primary Hematology Histone-Lysine N-Methyltransferase biochemical phenomena metabolism and nutrition medicine.anatomical_structure KMT2A Oncology Notch proteins 030220 oncology & carcinogenesis Child Preschool Pediatrics Perinatology and Child Health Chromosome Inversion Cancer research biology.protein Trans-Activators business Myeloid-Lymphoid Leukemia Protein 030215 immunology |
| Zdroj: | Journal of pediatric hematology/oncology. 42(4) |
| ISSN: | 1536-3678 |
| Popis: | T-cell therapy-related acute lymphoblastic leukemia (T-t-ALL) is a rare condition associated with previous cytotoxic therapy for another disease. Here we report T-t-ALL with inv(11)(q21q23), which involves KMT2A and MAML2, a transcriptional coactivator of NOTCH proteins, that occurred after chemotherapy for Philadelphia chromosome-positive B-cell acute lymphoblastic leukemia. This case describes the youngest patient with T-t-ALL harboring inv(11)(q21q23) and is the first independent report following an initial series also occurring in children. Our results lend further support to the observation that the KMT2A-MAML2 fusion gene resulting from inv(11)(q21q23) is likely a recurrent cytogenetic abnormality in T-t-ALL and appears to be associated with pediatric cases. |
| Databáze: | OpenAIRE |
| Externí odkaz: |
|